68 research outputs found

    A lineage-specific Exo70 is required for receptor kinase-mediated immunity in barley

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    In the evolution of land plants, the plant immune system has experienced expansion in immune receptor and signaling pathways. Lineage-specific expansions have been observed in diverse gene families that are potentially involved in immunity but lack causal association. Here, we show that Rps8-mediated resistance in barley to the pathogen Puccinia striiformis f. sp. tritici (wheat stripe rust) is conferred by a genetic module: Pur1 and Exo70FX12, which are together necessary and sufficient. Pur1 encodes a leucine-rich repeat receptor kinase and is the ortho-log of rice Xa21, and Exo70FX12 belongs to the Poales-specific Exo70FX clade. The Exo70FX clade emerged after the divergence of the Bromeliaceae and Poaceae and comprises from 2 to 75 members in sequenced grasses. These results demonstrate the requirement of a lineage-specific Exo70FX12 in Pur1-mediated immunity and sug-gest that the Exo70FX clade may have evolved a specialized role in receptor kinase signalin

    Particle Film Technology: approach for a biorational control of Cacopsylla pyri (Rhynchota Psyllidae) in Northern Italy

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    Two trials were carried out to investigate the efficacy of a kaolin-based product (Surround WP) a white non-abrasive, finegrained alluminum-silicate mineral in controlling pear psylla Cacopsylla pyri (L.) oviposition. The trial was carried out in Italy’s Emilia-Romagna Region on cv. Abbè Fétel during late winter in 2001-2002 year; the reference product was mineral oil. The timing of product application was before or at the onset of egg laying during overwintering. The results show a very good efficacy of kaolin in comparison to the mineral oil and untreated control. No eggs were found on the treated plants and no phytotoxic effects were observed. No nymphs were observed inside the flowers in the kaolin-treated plots

    HFE gene mutations and Wilson's disease in Sardinia

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    BACKGROUND: Hypocaeruloplasminaemia can lead to tissue iron storage in Wilson's disease and the possibility of iron overload in long-term overtreated patients should be considered. The HFE gene encodes a protein that is intimately involved in intestinal iron absorption. AIMS: The aim of this study was to determine the prevalence of the HFE gene mutation, its role in iron metabolism of Wilson's disease patients and the interplay of therapy in copper and iron homeostasis. METHODS: The records of 32 patients with Wilson's disease were reviewed for iron and copper indices, HFE gene mutations and liver biopsy. RESULTS: Twenty-six patients were negative for HFE gene mutations and did not present significant alterations of iron metabolism. The HFE mutation was significantly associated with increased hepatic iron content (P<0.02) and transferrin saturation index (P<0.03). After treatment period, iron indices were significantly decreased only in HFE gene wild-type. CONCLUSIONS: The HFE gene mutations may be an addictional factor in iron overload in Wilson's disease. Our results showed that an adjustment of dosage of drugs could prevent further iron overload induced by overtreatment only in patients HFE wild-type

    Non-invasive assessment of hepatic fibrosis in a series of patients with Wilson's Disease

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    BACKGROUND/AIMS: Liver biopsy has always represented the standard of reference in hepatic fibrosis assessment. Recently, blood markers and instrumental methods have been proposed for non-invasive assessment. The aim of this study was to validate transient elastography and other non-invasive tests compared to liver histology in Wilson's Disease. METHODS: Liver stiffness in 35 Wilson's Disease patients was evaluated by Fibroscan, serum fibrosis markers (AST-to-platelet-ratio index and FIB-4) and biopsy. RESULTS: Compared to liver histology, the FibroScan values increased proportionally with progression of the histological fibrosis stage. Significant fibrosis could be predicted with a Fibroscan cut-off value of 6.6 kPa. Advanced fibrosis could be predicted with a FibroScan cut-off value of 8.4 kPa. Serum fibrosis marker values gave good correlation with hepatic stage. CONCLUSIONS: A FibroScan value of 6.6 kPa was found to be a significant separation limit for differentiating significant fibrosis stages from milder stages and a fibroscan value of 8.4 kPa was found to be a significant separation limit for differentiating advanced fibrosis stages from milder stages. FibroScan values are clinically useful for predicting fibrosis stages and helpful in managing chronic therapy in Wilson's Disease patients
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